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Sarnak and colleagues (1) concluded that a low target blood pressure slowed the progression of nondiabetic kidney disease. However, Ruggenenti and associates (2) recently reported that no additional benefit from further blood pressure reduction by felodipine (dihydropyridine calcium-channel blockers) could be shown in patients with nondiabetic proteinuric nephropathies receiving background angiotensin-converting enzyme (ACE) inhibitor therapy. As Sarnak and colleagues pointed out, more participants in the low target blood pressure group received ACE inhibitors in their study (1). Angiotensin-converting enzyme inhibitors are known to slow progression of kidney disease independently of their blood pressure–lowering effect (3). In the African-American Study of Kidney Disease and Hypertension, targeting antihypertensive therapy at a mean blood pressure of 92 mm Hg compared with usual targets of 102 to 107 mm Hg did not slow progression of hypertensive nephrosclerosis (4). In that study, an identical proportion of patients in the usual and lower blood pressure groups were taking ACE inhibitors (4). In the study by Ruggenenti and associates (2), the proportion of participants receiving ramipril in both the conventional (diastolic blood pressure <90 mm Hg) and intensified (target blood pressure 130/80 mm Hg) blood pressure groups was identical in order to measure the pure effect of lowering blood pressure by felodipine on the progression of kidney disease. Therefore, although Sarnak and colleagues' sensitivity analysis did not affect their results, their conclusion that blood pressure reduction confers an additional renoprotective effect remains questionable.